Bottom Line:
Human infection caused by Shewanella algae is rare, which usually occurred after direct contact with seawater or ingestion of raw seafood in the immunocompromised host.Here, we report a fatal case of spontaneous bacterial peritonitis with bacteremia due to S. algae in a 57-year-old male with liver cirrhosis who had no history of exposure to seawater or raw seafood.Polymicrobial infection with Streptococcus mitis and Escherichia coli was combined and the patient died in spite of early appropriate antimicrobial therapy and early goal-directed therapy for sepsis.

Affiliation: Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Korea.

ABSTRACTHuman infection caused by Shewanella algae is rare, which usually occurred after direct contact with seawater or ingestion of raw seafood in the immunocompromised host. There have been anecdotal reports about Shewanella infections in human, but their pathogenic role and microbiologic data are limited. Here, we report a fatal case of spontaneous bacterial peritonitis with bacteremia due to S. algae in a 57-year-old male with liver cirrhosis who had no history of exposure to seawater or raw seafood. Polymicrobial infection with Streptococcus mitis and Escherichia coli was combined and the patient died in spite of early appropriate antimicrobial therapy and early goal-directed therapy for sepsis.

Mentions:
A 57-year-old male was transferred to the emergency department after endoscopic hemostasis for 1,000 mL of massive hematemesis due to esophageal and cardiac variceal bleeding. The patient had been diagnosed with alcoholic LC with varices 1 year ago. The patient was taking propranolol for varices and metformin for diabetes. The patient had no history of travel, no contact with seawater or fresh water, and did not consume raw fish within the last 6 months. On physical examination, the blood pressure was 100/40 mmHg, heart rate was 176 beats/min, respiration rate was 28/min and body temperature was 35℃. The mental state was alert but confused and icteric sclerae were observed. The heart sound was regular without murmur, and the breathing sound was clear. The abdomen was distended with decreased bowel sounds. Complete blood count showed white blood cells (WBC) counts of 12,960/mm3 (neutrophils, 78%), hemoglobin levels of 5.7 g/dL, and platelet counts of 46,000/mm3. A coagulation test showed a prothrombin time (PT) of 22.8 seconds (33.8%, INR 2.04) and an activated partial thromboplastin time of 58.7 seconds. Blood chemistry showed the following: aspartate aminotransferase/alanine aminotransferase 522/103 IU/L, total bilirubin/direct bilirubin 3.21/1.18 mg/dL, total protein/albumin 4.3/2.29 g/dL, creatine phosphokinase/lactate dehydrogenase 281/2,358 IU/L, blood urea nitrogen/creatinine 14.0/0.96 mg/dL, sodium/potassium 152/3.9 mmol/L. Serum osmolarity was 349 mOsm/kg, lactic acid was 119.5 mg/dL (1-13 mg/dL) and highly sensitive C-reactive protein (hsCRP) was 29.34 mg/L. Arterial blood gas analysis under 4 L of oxygen via nasal cannula revealed a pH of 7.19, PaCO2 of 15.6 mmHg, PaO2 of 109.5 mmHg, HCO3- of 5.9 mmol/L, and oxygen saturation of 97.3%, which represented metabolic acidosis with an anion gap of 35.1. Chest X-ray was normal but, abdominal X-ray showed moderate ascites and paralytic ileus (Fig. 1A). Because of persistent hemodynamic instability, we could not perform endoscopic hemostasis. Instead, we inserted a Sengstaken Blakemore (SB) tube. On the second hospital day (HD), the patient had a fever up to 40℃ and showed decreased mentality. To exclude SBP, we performed ascites tapping. The ascites fluid analysis revealed WBC counts of 5,800/mm3 (neutrophils, 93%), albumin levels of 0.43 g/dL and the serum-ascites albumin gradient of 2.24, which agreed with SBP. We initiated cefotaxime (6 g/day) and metronidazole (1,500 mg/day) and continued early goal-directed therapy (EGDT) for sepsis. On the third HD, the patient was intubated and underwent mechanical ventilation. Based on the follow-up chest X-ray (Fig. 1B) and clinical course, we assessed the patient having the respiratory failure which was combined with pulmonary edema due to massive hydration and transfusion for gastrointestinal bleeding and aspiration related to hematemesis. On the third HD, the blood culture revealed growth of Gram-positive cocci and Gram-negative bacilli. We added gentamicin (160 mg/day) because we could not exclude the possibility of infective endocarditis. Using the Microscan system (Siemens, Inc., Renton, WA, USA), Shewanella spp. and S. mitis were isolated from both peripheral and central blood (4 of 4 bottles) and Shewanella spp. and E. coli were isolated from ascites. S. mitis was susceptible to penicillin and E. coli was susceptible to all of the antibiotics including ampicillin, cefotaxime, levofloxacin and gentamicin. The Shewanella isolate was sub-cultured on MacConkey agar at 37℃, and growth was found after 16 hours of incubation. Based on the API 20NE kit (bioMérieux Inc., Marcy-l'Etoile, France), the organism was identified as S. putrefaciens with 99.9% certainty. We performed additional biochemical tests, as well as 16S rRNA PCR with sequencing analysis because it is known that an automatic bacterial culture system and biochemical identification system, such as ID32E, ID32GN, or API 20E could not distinguish S. algae from S. putrefaciens [2]. The isolate was incubated on sheep blood agar and showed growth at 42℃ (but not 4℃) and on nutrient agar containing 6.5% NaCl, which was compatible with S. algae. 16S rRNA gene sequencing analysis was performed with the following primers [4]: HDA1 forward primer (5'-ACTCCTACGGGAGGCAGCAGT-3') and HDA2 reverse primer (5'-GTATTACCGCGGCTGCTGGCA-3'). The isolate gene sequence showed 100% concordance with the S. algae strain QC39 (GenBank accession number: JN384129). S. mitis was susceptible to penicillin, and S. algae was susceptible to piperacillin, cefotaxime, ceftazidime, cefepime, carbapenems, aminoglycosides and quinolones. A transthoracic echocardiogram showed no evidence of vegetation. Because the patient had persistent fever, leukocytosis, and elevated hsCRP with progressing pneumonia, we changed the antibiotics to piperacillin/tazobactam (12/1.5 g/day) and amikacin (500 mg/day) on the 9th HD, which could reinforce the antimicrobial activity for nosocomial pathogens such as Pseudomonas. After then, fever subsided and clinical condition was improved with normalization of WBC and hsCRP levels. Follow-up culture of ascites on the 8th HD and blood on the 13th HD, showed no bacterial pathogens. Amikacin was discontinued on the 15th HD. The SB tube was removed on the 16th HD. However, hepatic failure was progressing with total bilirubin up to 30.84 md/dL and prolonged PT to 34.3 seconds (21.8%). Urine volume decreased below 500 mL/day despite diuretics use. Metabolic acidosis due to renal failure worsened and the mental state remained confused. Hepatorenal syndrome was suspected and planned dialysis was proposed, but his family refused further treatment. He died on the 19th HD.

Mentions:
A 57-year-old male was transferred to the emergency department after endoscopic hemostasis for 1,000 mL of massive hematemesis due to esophageal and cardiac variceal bleeding. The patient had been diagnosed with alcoholic LC with varices 1 year ago. The patient was taking propranolol for varices and metformin for diabetes. The patient had no history of travel, no contact with seawater or fresh water, and did not consume raw fish within the last 6 months. On physical examination, the blood pressure was 100/40 mmHg, heart rate was 176 beats/min, respiration rate was 28/min and body temperature was 35℃. The mental state was alert but confused and icteric sclerae were observed. The heart sound was regular without murmur, and the breathing sound was clear. The abdomen was distended with decreased bowel sounds. Complete blood count showed white blood cells (WBC) counts of 12,960/mm3 (neutrophils, 78%), hemoglobin levels of 5.7 g/dL, and platelet counts of 46,000/mm3. A coagulation test showed a prothrombin time (PT) of 22.8 seconds (33.8%, INR 2.04) and an activated partial thromboplastin time of 58.7 seconds. Blood chemistry showed the following: aspartate aminotransferase/alanine aminotransferase 522/103 IU/L, total bilirubin/direct bilirubin 3.21/1.18 mg/dL, total protein/albumin 4.3/2.29 g/dL, creatine phosphokinase/lactate dehydrogenase 281/2,358 IU/L, blood urea nitrogen/creatinine 14.0/0.96 mg/dL, sodium/potassium 152/3.9 mmol/L. Serum osmolarity was 349 mOsm/kg, lactic acid was 119.5 mg/dL (1-13 mg/dL) and highly sensitive C-reactive protein (hsCRP) was 29.34 mg/L. Arterial blood gas analysis under 4 L of oxygen via nasal cannula revealed a pH of 7.19, PaCO2 of 15.6 mmHg, PaO2 of 109.5 mmHg, HCO3- of 5.9 mmol/L, and oxygen saturation of 97.3%, which represented metabolic acidosis with an anion gap of 35.1. Chest X-ray was normal but, abdominal X-ray showed moderate ascites and paralytic ileus (Fig. 1A). Because of persistent hemodynamic instability, we could not perform endoscopic hemostasis. Instead, we inserted a Sengstaken Blakemore (SB) tube. On the second hospital day (HD), the patient had a fever up to 40℃ and showed decreased mentality. To exclude SBP, we performed ascites tapping. The ascites fluid analysis revealed WBC counts of 5,800/mm3 (neutrophils, 93%), albumin levels of 0.43 g/dL and the serum-ascites albumin gradient of 2.24, which agreed with SBP. We initiated cefotaxime (6 g/day) and metronidazole (1,500 mg/day) and continued early goal-directed therapy (EGDT) for sepsis. On the third HD, the patient was intubated and underwent mechanical ventilation. Based on the follow-up chest X-ray (Fig. 1B) and clinical course, we assessed the patient having the respiratory failure which was combined with pulmonary edema due to massive hydration and transfusion for gastrointestinal bleeding and aspiration related to hematemesis. On the third HD, the blood culture revealed growth of Gram-positive cocci and Gram-negative bacilli. We added gentamicin (160 mg/day) because we could not exclude the possibility of infective endocarditis. Using the Microscan system (Siemens, Inc., Renton, WA, USA), Shewanella spp. and S. mitis were isolated from both peripheral and central blood (4 of 4 bottles) and Shewanella spp. and E. coli were isolated from ascites. S. mitis was susceptible to penicillin and E. coli was susceptible to all of the antibiotics including ampicillin, cefotaxime, levofloxacin and gentamicin. The Shewanella isolate was sub-cultured on MacConkey agar at 37℃, and growth was found after 16 hours of incubation. Based on the API 20NE kit (bioMérieux Inc., Marcy-l'Etoile, France), the organism was identified as S. putrefaciens with 99.9% certainty. We performed additional biochemical tests, as well as 16S rRNA PCR with sequencing analysis because it is known that an automatic bacterial culture system and biochemical identification system, such as ID32E, ID32GN, or API 20E could not distinguish S. algae from S. putrefaciens [2]. The isolate was incubated on sheep blood agar and showed growth at 42℃ (but not 4℃) and on nutrient agar containing 6.5% NaCl, which was compatible with S. algae. 16S rRNA gene sequencing analysis was performed with the following primers [4]: HDA1 forward primer (5'-ACTCCTACGGGAGGCAGCAGT-3') and HDA2 reverse primer (5'-GTATTACCGCGGCTGCTGGCA-3'). The isolate gene sequence showed 100% concordance with the S. algae strain QC39 (GenBank accession number: JN384129). S. mitis was susceptible to penicillin, and S. algae was susceptible to piperacillin, cefotaxime, ceftazidime, cefepime, carbapenems, aminoglycosides and quinolones. A transthoracic echocardiogram showed no evidence of vegetation. Because the patient had persistent fever, leukocytosis, and elevated hsCRP with progressing pneumonia, we changed the antibiotics to piperacillin/tazobactam (12/1.5 g/day) and amikacin (500 mg/day) on the 9th HD, which could reinforce the antimicrobial activity for nosocomial pathogens such as Pseudomonas. After then, fever subsided and clinical condition was improved with normalization of WBC and hsCRP levels. Follow-up culture of ascites on the 8th HD and blood on the 13th HD, showed no bacterial pathogens. Amikacin was discontinued on the 15th HD. The SB tube was removed on the 16th HD. However, hepatic failure was progressing with total bilirubin up to 30.84 md/dL and prolonged PT to 34.3 seconds (21.8%). Urine volume decreased below 500 mL/day despite diuretics use. Metabolic acidosis due to renal failure worsened and the mental state remained confused. Hepatorenal syndrome was suspected and planned dialysis was proposed, but his family refused further treatment. He died on the 19th HD.

Bottom Line:
Human infection caused by Shewanella algae is rare, which usually occurred after direct contact with seawater or ingestion of raw seafood in the immunocompromised host.Here, we report a fatal case of spontaneous bacterial peritonitis with bacteremia due to S. algae in a 57-year-old male with liver cirrhosis who had no history of exposure to seawater or raw seafood.Polymicrobial infection with Streptococcus mitis and Escherichia coli was combined and the patient died in spite of early appropriate antimicrobial therapy and early goal-directed therapy for sepsis.

Affiliation:
Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Korea.

ABSTRACTHuman infection caused by Shewanella algae is rare, which usually occurred after direct contact with seawater or ingestion of raw seafood in the immunocompromised host. There have been anecdotal reports about Shewanella infections in human, but their pathogenic role and microbiologic data are limited. Here, we report a fatal case of spontaneous bacterial peritonitis with bacteremia due to S. algae in a 57-year-old male with liver cirrhosis who had no history of exposure to seawater or raw seafood. Polymicrobial infection with Streptococcus mitis and Escherichia coli was combined and the patient died in spite of early appropriate antimicrobial therapy and early goal-directed therapy for sepsis.